Association between cigarette smoking and erectile tumescence: the mediating role of heart rate variability.

Cigarette smoking deleteriously affects erectile function, and conversely, quitting smoking improves erectile hemodynamics. Underlying mechanisms by which smoking (or reduction of smoking frequency) may affect erectile physiology are not well understood. This study examined the mediating role of heart rate variability (HRV; a marker of sympathovagal balance) among a sample of male chronic smokers from the United States. Sixty-two healthy men (Mage=38.27 years; s.d.=10.62) were assessed at baseline (while smoking regularly), at mid-treatment (while using a nicotine patch) and at follow-up, 4 weeks after patch discontinuation. Cigarette use, frequency-domain parameters of HRV (low frequency (LF), high frequency (HF), LF/HF ratio) and physiological sexual arousal responses (via penile plethysmography) were assessed at each visit. Results were consistent with mediation, in that greater reductions in cigarette use from baseline to follow-up were associated with longitudinal increases in LF, which in turn showed positive relationships with across-time changes in erectile tumescence. Neither HF nor LF/HF ratio mediated the relationship between smoking and erection. In conclusion, HRV mediated the inverse relationship between reductions in smoking and enhancements in erectile tumescence. Results underscore the possibility that cigarette use may deleteriously affect erectile function peripherally, in part, by disrupting cardiac autonomic function.